Diabetic Ketoacidosis

Acute management

A state of Absolute Insulin Bankruptcy

ICU subposting presentation

Gwen Lim
 Lab Investigations
• Diagnosis
• Delineate Etiology
• Therapy and monitoring

• FBC, Blood Glucose, Serum Na & K,

• Urea and Creatininte
• Urine FEME (glycosuria and ketoua)
• ABG (pH, HCO3)
• Plasma Ketones
• Causes: CXR, infective screen, ECG, Urine microscopy
Precipitating factors
 Infection

 missed therapy

 Acute coronary syndrome

 CVA

 Surgery
 Diagnostic criteria

All three must be met

• Capillary blood glucose >11 mmol/L

• Capillary ketones >3 mmol/L or urine ketones >2+

• Venous pH <7.3 and/or bicarbonate <15 mmol/L

 High-dependency unit (HDU) admission

• Elderly
• Pregnant ladies
• Heart or kidney failure
• Other serious comorbidities
• Severe DKA by following criteria:
– Venous bicarbonate <5 mmol/L
– Blood ketones >6 mmol/L
– Venous pH <7.1
– Hypokalaemia on admission (<3.5 mmol/L)
– Glasgow Coma Scale (GCS) <12
– Oxygen saturation <92% on air (arterial blood gases required)
– Systolic BP <90 mm Hg
– Pulse >100 or <60 beats/minute
– Anion gap >16
Anion Gap = (Na+ K) – (Cl + HCO3-)
 Management
FLuid loss Electrolytes

Hyperglycemia Acidosis

Precipitating
Factor

Step 1. Commence 0.9% NS drip
Step 2. Commence a fixed rate
intravenous insulin infusion (IVII)
Step 3. Assess patient
Step 4
Investigations
Step 5
Outline monitoring regimen
Step 6. Look for precipitating
causes and treat accordingly
1st Hour: Immediate Management
using large bore cannula.
(0.1 unit/kg/hr based on estimate of weight).
1U/mls short-acting human insulin in 0.9% NS solution.
• BP, Pulse, Temperature, Respiratory rate, Oxygen saturation
• Glasgow Coma Scale
• Hydration status
• Full clinical examination
• Capillary and venous blood glucose
• Arterial blood gases
• Blood or urinary ketones
• BUSE, FBC
• Blood cultures, MSU
• ECG (if indicated)
• CXR (if indicated)
Hourly capillary blood glucose
• VS and IO charting hourly
• HCO3 and K level at 60 minutes,
4 hours and 6-hourly thereafter
• 6-hourly BUSE and urine ketone
• Continuous SpO2 (if indicated)
• Continuous cardiac monitoring (if indicated)
Start broad-spectrum antibiotics if infection suspected
use with caution
Fluids commencement
Potassium replacement
 HCO3

• The use of IV Bicarbonate is not indicated

to correct acidosisin DKA

• Rise in pCO2 in CSF which may lead to a paradoxical

increase in CSF acidosis.
• Delay in the fall of blood lactate and ketone level.
• Risk of cerebral oedema especially in younger age
groups.
 Aims of treatment: 2nd to 6th Hour
• Rate of fall of ketones of at least 0.5 mmol/L/hr, or

• Bicarbonate rise 3 mmol/L/hr, and

• Blood glucose fall 3 mmol/L/hr ( Avoid hypoglycaemia)

• Maintain serum potassium in normal range

 Management: 2nd to 6th Hour
• Step 7. Reassess patient, monitor vital signs

• Step 8 Continue fluid replacement via infusion pump as follows:

– 1 litre of 0.9% saline with KCL over next 2 hours
– 1 litre of 0.9% saline with KCL over next 4 hours
– Once blood glucose falls below 14 mmol/L:
• Switch to 5% dextrose at 125 mL/hr and reduce insulin
infusion rate to 0.05 units/kg/hour; or
• Switch to 10% dextrose at 125 mL/hr with no change in
insulin infusion rate.
– More cautious fluid replacement in young people aged under 18
years, elderly, pregnant, have heart or renal failure (Consider
HDU and central line)

• Step 9. Assess response to treatment

– Continue fixed rate IVII until ketones less than 0.3 mmol/L,
venous pH over 7.3 and/or venous bicarbonate over 18mmol/L
 Aims of treatment: 6th to 12th Hour
• Ensure clinical and biochemical parameters improving

• Continue IV fluid replacement

• Avoid hypoglycaemia

• Assess for complications of treatment e.g. fluid

overload, cerebral oedema

• Treat precipitating factors as necessary

 Management: 6th to 12th Hour
• Step 10 Reassess patient, monitor vital signs
– Continue IV fluid at reduced rate
• 1000 mL of 0.9% saline with potassium chloride over 4 hours
(continuation from the 5th hour)
• 1000 mL of 0.9% saline with potassium chloride over 8 hours
– Once blood glucose falls below 14 mmol/L:
» Switch to 5% dextrose at 125 mL/hr and reduce insulin
infusion rate to 0.05 units/kg/hour; or
» Switch to 10% dextrose at 125 mL/hr with no change in
insulin infusion rate.
– Reassess cardiovascular status at 12 hours; further fluid may be
required, check for fluid overload
• Step 11. Review biochemical and metabolic parameters
– At 6 hours check venous pH, bicarbonate, potassium, blood ketones
and glucose
• Resolution is defined as: Blood ketones <0.3 mmol/L, Venous pH >7.3
(do not use bicarbonate as a surrogate at this stage)
If DKA not resolved review insulin infusion (see Step 9)
• If DKA resolved go to BOX entitled Resolution of DKA
 Management: 12th - 24th Hour
Aim:
• Ensure that clinical and biochemical parameters are continuing to
improve or are normal
• Continue IVD if not eating and drinking
• If ketonaemia cleared and patient is not eating and drinking, titrate insulin
infusion rate accordingly
• Reassess for complications of treatment e.g. fluid overload, cerebral
oedema
• Continue to treat precipitating factors
• Change to subcutaneous insulin if patient is eating and drinking normally

Step 12. Reassess patient, monitor vital signs, review biochemical and
metabolic parameters
• At 12 hours check venous pH, bicarbonate, potassium, capillary ketones
and glucose
• If not resolved review Step 9 and Step 10.
If DKA resolved go below
 Resolution of DKA
Expectation:
Patient should be eating and drinking and back on normal insulin
• If DKA is not resolved identify and treat the reasons for failure to
respond
• Convert to subcutaneous regime when biochemically stable (blood
ketones <0.3 mmol/L, pH >7.3) and the patient is ready and
able to eat.

Do not discontinue intravenous insulin infusion until 30 minutes after

subcutaneous short acting insulin has been given.

Calculating subcutaneous insulin dose in insulin-naïve patients;

Calculating a Basal Bolus (QID) Regimen.
 Estimate Total Daily Dose (TDD) of Insulin

TDD: Weight (in kg) x 0.5 - 0.75 units.

• Use 0.75 units/kg for those thought to be more insulin
resistant e.g. obese, acanthosis nigricans

• Example: a 80 kg person would require approximately 80

x 0.5 units or 40 units in 24 hours
• Give 50% of total dose at bedtime in the form of long
acting insulin and divide remaining dose equally between
prebreakfast,
• pre-lunch and pre-evening meal.
• E.g. Short-acting insulin 7u tid & 20 units bedtime
 Important notes
• Measurement of blood ketones when available as opposed to urine ketones
• Measurement of venous pH as opposed to arterial blood gases (ABG - arterial blood
gas only if pO2 or pCO2 measurement is required)
• Crystalloid solution sodium chloride 0.9% to be used as opposed to Hartmann solution
• A priming dose of insulin is not necessary, in the treatment of DKA, provided that the
insulin infusion is started promptly at a dose of 0.1 unit per kg per hour.
• Replacing `sliding scale` insulin with a weight-based fixed-rate intravenous insulin
infusion. A fixed insulin regimen of 0.1unit per kg per hour to be used for at least the
first 6 – 12 hours of therapy. A traditional lower-dose variable rate insulin infusion(VRII)*
to be used once ketonaemia has cleared.
• Remember that 0.1unit per kg per hour is a relatively concentrated solution of insulin
and prevention of hypoglycaemia is paramount.
• At least 2 venflons: Use both arms with a venflon in each arm. One side is for the
sodium chloride 0.9% infusion with the insulin infusion piggy-backed. The other side is
for the 10% glucose infusion, once the blood glucose has fallen to < 14 mmol/l.
• When the glucose infusion is commenced, it is given as well as sodium chloride, not in
place of sodium chloride.
• Continue long-acting analogue insulin e.g. Lantus/Levemir at its usual dose.
• Potassium replacement is given through the sodium chloride 0.9% arm not glucose arm
• Do not give bicarbonate without senior consultant approval
 REFERENCES

http://www.cmft.nhs.uk/media/383957/dka%20guidelines%20-%202012.pdf
 Additional reading

https://emcrit.org/pulmcrit/blood-gas-measurements-dka-searching-unicorn/
• obesity itself causes some degree of insulin resistance. Patients who are not obese
by traditional weight criteria may have an increased percentage of body fat distributed
predominantly in the abdominal region. Ketoacidosis seldom occurs spontaneously in
this type of diabetes; when seen, it usually arises in association with the stress of
another illness such as infection. This form of diabetes frequently goes undiagnosed
for many years because the hyperglycemia develops gradually and at earlier stages
is often not severe enough for the patient to notice any of the classic symptoms of
diabetes. Nevertheless, such patients are at increased risk of developing
macrovascular and microvascular complications. Whereas patients with this form of
diabetes may have insulin levels that appear normal or elevated, the higher blood
glucose levels in these diabetic patients would be expected to result in even higher
insulin values had their β-cell function been normal. Thus, insulin secretion is
defective in these patients and insufficient to compensate for insulin resistance.
Insulin resistance may improve with weight reduction and/or pharmacological
treatment of hyperglycemia but is seldom restored to normal. The risk of developing
this form of diabetes increases with age, obesity, and lack of physical activity. It
occurs more frequently in women with prior GDM and in individuals with hypertension
or dyslipidemia, and its frequency varies in different racial/ethnic subgroups. It is often
associated with a strong genetic predisposition, more so than is the autoimmune form
of type 1 diabetes. However, the genetics of this form of diabetes are complex and
not clearly defined.
 acetoacetate vs 3-beta-hydroxybutyrate

• +, ++ and +++ corresponded to median

capillary blood ketone levels of
• 0.5 mmol/l (IQR: 0.1-0.9), 0.7 mmol/l (IQR:
0.2-1.8) and 3 mmol/l (IQR: 1.4-5.2), r
 The case for venous rather than arterial blood
gases in diabetic ketoacidosis.
• In patients with DKA the weighted average difference between
arterial and venous pH was 0.02 pH units (95% limits of agreement
-0.009 to +0.021 pH units) and between arterial and venous
bicarbonate was -1.88 mEq/L.

• CONCLUSIONS:
There is reasonable evidence that venous and arterial pH have
sufficient agreement as to be clinically interchangeable in patients with
DKA who are haemodynamically stable and without respiratory failure.
There is some evidence that venous and arterial bicarbonate also
agree closely in DKA

Arterial blood gas determinations in patients with suspected diabetic

ketoacidosis (DKA) are time-consuming, expensive, and painful.